INI-CET 2010

Q: A dead body is having cadaveric lividity of bluish green color. The most likely cause of death is by poisoning due to:

Hydrogen sulfide. ***Hydrogen sulfide*** - **Hydrogen sulfide poisoning** classically causes a **bluish-green cadaveric lividity** due to the formation of sulfhemoglobin. - This distinct discoloration is a key indicator often noted during post-mortem examination in cases of hydrogen sulfide exposure. *Hydrocyanic acid* - **Hydrocyanic acid poisoning** typically leads to a **cherry-red lividity** due to the inhibition of cytochrome oxidase, preventing tissue oxygen utilization, which is different from the bluish-green color described. - The bright red color results from the persistence of oxygenated hemoglobin in the venous blood. *Oleander* - **Oleander poisoning** affects the heart, causing **cardiac arrhythmias** and bradycardia, but does not typically produce a characteristic or distinct cadaveric discoloration like the bluish-green hue. - Lividity would generally be a more typical reddish-purple, consistent with simple hypostasis. *Sodium nitrite* - **Sodium nitrite poisoning** causes **methemoglobinemia**, leading to a characteristic **chocolate-brown or grayish-blue lividity** due to the oxidation of hemoglobin, which differs from the specific bluish-green described. - This change is due to the formation of methemoglobin, which cannot carry oxygen effectively. [Practice more INI-CET 2010 questions on OnCourse]

Q: Commonest cause of thunderclap headache:

Aneursymal SAH. ***Aneursymal SAH*** - An **aneurysmal subarachnoid hemorrhage (SAH)** is the most common and often life-threatening cause of a **thunderclap headache**, characterized by a sudden, severe headache reaching maximum intensity within one minute [1]. - The sudden rupture of a cerebral aneurysm leads to blood spilling into the subarachnoid space, causing a rapid increase in intracranial pressure and meningeal irritation. *Basilar migraine* - While basilar migraine can cause severe headaches, it typically presents with neurological symptoms like **vertigo**, **ataxia**, and **diplopia** preceding the headache phase, and its onset is usually less abrupt than a thunderclap headache. - Basilar migraines usually have a **recurrent pattern** and are associated with a history of similar migraine episodes, unlike the abrupt, singular nature of an SAH-related thunderclap headache. *Extradural hemorrhage* - An **extradural (epidural) hemorrhage** is usually caused by **head trauma** and often presents with a **lucid interval** followed by a progressive neurological decline, rather than an immediate thunderclap headache [2]. - It involves bleeding between the **dura mater** and the skull, which typically develops more slowly than the catastrophic onset of an SAH. *Subdural hemorrhage* - A **subdural hemorrhage** is usually caused by **venous bleeding** and can be acute, subacute, or chronic, often presenting with a gradual onset of symptoms like headache, confusion, and neurological deficits [2]. - While an acute subdural hematoma can be severe, its headache is generally not as instantaneously explosive or universally described as a thunderclap as that seen with SAH. [Practice more INI-CET 2010 questions on OnCourse]

Q: Which of the following substances is not classified as an opioid?

Ketamine. ***Ketamine*** - **Ketamine** is classified as a **dissociative anesthetic** and does not act on opioid receptors. - Its primary mechanism of action involves **N-methyl-D-aspartate (NMDA) receptor antagonism**. *Heroin* - **Heroin** (diacetylmorphine) is a **semisynthetic opioid** derived from morphine [1, 3]. - It rapidly crosses the **blood-brain barrier** and is metabolized to morphine, where it acts as a potent **mu-opioid receptor agonist** [3]. *Methadone* - **Methadone** is a **synthetic opioid** used in the treatment of opioid dependence and chronic pain [1, 2]. - It acts primarily as a **mu-opioid receptor agonist** with a long duration of action [1, 2]. *Fentanyl* - **Fentanyl** is a powerful **synthetic opioid** analgesic, much more potent than morphine [2]. - It selectively binds to and activates **mu-opioid receptors**, producing strong analgesic and sedative effects [2]. [Practice more INI-CET 2010 questions on OnCourse]

4 Previous Year Questions with Answers & Explanations

Questions

Subjects

All (4)Forensic Medicine (1)Internal Medicine (1)Pathology (1)Pharmacology (1)

Forensic Medicine

1 questions

A dead body is having cadaveric lividity of bluish green color. The most likely cause of death is by poisoning due to:

INI-CET 2010 - Forensic Medicine INI-CET Practice Questions and MCQs

Question 1: A dead body is having cadaveric lividity of bluish green color. The most likely cause of death is by poisoning due to:

A. Hydrogen sulfide (Correct Answer)
B. Hydrocyanic acid
C. Oleander
D. Sodium nitrite

Explanation: ***Hydrogen sulfide*** - **Hydrogen sulfide poisoning** classically causes a **bluish-green cadaveric lividity** due to the formation of sulfhemoglobin. - This distinct discoloration is a key indicator often noted during post-mortem examination in cases of hydrogen sulfide exposure. *Hydrocyanic acid* - **Hydrocyanic acid poisoning** typically leads to a **cherry-red lividity** due to the inhibition of cytochrome oxidase, preventing tissue oxygen utilization, which is different from the bluish-green color described. - The bright red color results from the persistence of oxygenated hemoglobin in the venous blood. *Oleander* - **Oleander poisoning** affects the heart, causing **cardiac arrhythmias** and bradycardia, but does not typically produce a characteristic or distinct cadaveric discoloration like the bluish-green hue. - Lividity would generally be a more typical reddish-purple, consistent with simple hypostasis. *Sodium nitrite* - **Sodium nitrite poisoning** causes **methemoglobinemia**, leading to a characteristic **chocolate-brown or grayish-blue lividity** due to the oxidation of hemoglobin, which differs from the specific bluish-green described. - This change is due to the formation of methemoglobin, which cannot carry oxygen effectively.

Internal Medicine

1 questions

Commonest cause of thunderclap headache:

INI-CET 2010 - Internal Medicine INI-CET Practice Questions and MCQs

Question 1: Commonest cause of thunderclap headache:

A. Basilar migraine
B. Extradural hemorrhage
C. Subdural hemorrhage
D. Aneursymal SAH (Correct Answer)

Explanation: ***Aneursymal SAH*** - An **aneurysmal subarachnoid hemorrhage (SAH)** is the most common and often life-threatening cause of a **thunderclap headache**, characterized by a sudden, severe headache reaching maximum intensity within one minute [1]. - The sudden rupture of a cerebral aneurysm leads to blood spilling into the subarachnoid space, causing a rapid increase in intracranial pressure and meningeal irritation. *Basilar migraine* - While basilar migraine can cause severe headaches, it typically presents with neurological symptoms like **vertigo**, **ataxia**, and **diplopia** preceding the headache phase, and its onset is usually less abrupt than a thunderclap headache. - Basilar migraines usually have a **recurrent pattern** and are associated with a history of similar migraine episodes, unlike the abrupt, singular nature of an SAH-related thunderclap headache. *Extradural hemorrhage* - An **extradural (epidural) hemorrhage** is usually caused by **head trauma** and often presents with a **lucid interval** followed by a progressive neurological decline, rather than an immediate thunderclap headache [2]. - It involves bleeding between the **dura mater** and the skull, which typically develops more slowly than the catastrophic onset of an SAH. *Subdural hemorrhage* - A **subdural hemorrhage** is usually caused by **venous bleeding** and can be acute, subacute, or chronic, often presenting with a gradual onset of symptoms like headache, confusion, and neurological deficits [2]. - While an acute subdural hematoma can be severe, its headache is generally not as instantaneously explosive or universally described as a thunderclap as that seen with SAH.

Pathology

1 questions

Fetomaternal transfusion of fetal RBCs in mother can be detected by: UPSC 08; TN 08; AIIMS 10

INI-CET 2010 - Pathology INI-CET Practice Questions and MCQs

Question 1: Fetomaternal transfusion of fetal RBCs in mother can be detected by: UPSC 08; TN 08; AIIMS 10

A. Electrophoresis
B. Indirect Coomb's test
C. Direct Coomb's test
D. Betke-Kleihauer test (Correct Answer)

Explanation: ***Betke-Kleihauer test*** - The **Kleihauer-Betke test** (or acid elution test) detects fetal hemoglobin (HbF) in maternal blood. Fetal red blood cells, which contain HbF, are more resistant to acid elution and retain their hemoglobin, appearing stained, while adult red blood cells containing HbA lose their hemoglobin and appear as 'ghost' cells. - This visual differentiation allows for the quantification of **fetomaternal hemorrhage**, which is crucial for determining the appropriate dose of anti-D immunoglobulin in Rh-negative mothers [1]. - This is the **gold standard test** for detecting and quantifying fetomaternal transfusion. *Electrophoresis* - **Hemoglobin electrophoresis** is used to identify and quantify different types of hemoglobin (e.g., HbA, HbS, HbC, HbF) in a blood sample. While it can detect HbF, it is not the primary or most practical method for routinely quantifying the small percentage of fetal cells in maternal circulation in the context of fetomaternal hemorrhage. - It is typically used for diagnosing **hemoglobinopathies** and thalassemias, not for accurately determining the extent of fetomaternal transfusion. *Indirect Coombs test* - The **Indirect Coombs Test** (ICT) detects *antibodies circulating in the serum* that are capable of binding to red blood cells [1]. It is commonly used for **antibody screening** in prenatal care and for cross-matching blood transfusions. - While it can screen for maternal antibodies against fetal red blood cell antigens, it does not directly quantify the volume of fetal blood that has entered the maternal circulation. *Direct Coombs test* - The **Direct Coombs Test** (DCT) detects antibodies *attached directly to the surface of red blood cells*, typically indicating autoimmune hemolytic anemia or a hemolytic transfusion reaction. - It is used to detect antibodies on the infant's red blood cells in cases of **hemolytic disease of the newborn**, but not to quantify fetal cells in the mother's circulation. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 469-470.

Pharmacology

1 questions

Which of the following substances is not classified as an opioid?

INI-CET 2010 - Pharmacology INI-CET Practice Questions and MCQs

Question 1: Which of the following substances is not classified as an opioid?

A. Heroin
B. Ketamine (Correct Answer)
C. Methadone
D. Fentanyl

Explanation: ***Ketamine*** - **Ketamine** is classified as a **dissociative anesthetic** and does not act on opioid receptors. - Its primary mechanism of action involves **N-methyl-D-aspartate (NMDA) receptor antagonism**. *Heroin* - **Heroin** (diacetylmorphine) is a **semisynthetic opioid** derived from morphine [1, 3]. - It rapidly crosses the **blood-brain barrier** and is metabolized to morphine, where it acts as a potent **mu-opioid receptor agonist** [3]. *Methadone* - **Methadone** is a **synthetic opioid** used in the treatment of opioid dependence and chronic pain [1, 2]. - It acts primarily as a **mu-opioid receptor agonist** with a long duration of action [1, 2]. *Fentanyl* - **Fentanyl** is a powerful **synthetic opioid** analgesic, much more potent than morphine [2]. - It selectively binds to and activates **mu-opioid receptors**, producing strong analgesic and sedative effects [2].